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From metabolic neurotoxicity to hypoxic neuroprotection: an MRS study of cyclosporine role in rat brain

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Donohue P, Gottschalk,  S
Department High-Field Magnetic Resonance, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Citation

Serkova, N., Donohue P, Gottschalk, S., Hainz S, Christians, U., & Leibfritz, D. (2001). From metabolic neurotoxicity to hypoxic neuroprotection: an MRS study of cyclosporine role in rat brain. Poster presented at 9th Scientific Meeting of the International Society of Magnetic Resonance in Medicine (ISMRM), 18th Annual Meeting and Exhibition of the European Society for Magnetic Resonance in Medicine and Biology (ESMRMB), Glasgow, UK.


Abstract
Cyclosporine (CsA) is a major immunosuppressant after organ transplantation. To date, two controversial facts about CsA have been reported. Paradoxically, on one hand, CsA causes neurotoxicity via unknown mechanisms in up to 60 of transplant patients, which requires the withdrawal of CsA therapy. On the other hand, in contrast to its neurotoxic potential, significant neuroprotective effects against ischemia have been reported for CsA recently. It was speculated that whether CsA is neurotoxic or neuroprotective is concentrationdependent: high concentrations of CsA cause neurotoxicity, while concentrations below the therapeutic range are neuroprotective. Thus, it was our goal to evaluate and to compare the dose-dependent neurotoxic effects of CsA on rat brain metabolism in normoxia as well as its neuroprotective biochemical mechanisms under hypoxia.